Lithium diabetes insipidus with

Lithium reduces the kidney s ability to concentrate urine and may cause a nephrogenic diabetes insipidus with low urine specific gravity and low osmolality polyuria (urine volume greater than 3 L/day). This may be treated with loop diuretics, thiazide diuretics, or triamterene. If a thiazide diuretic is used, lithium doses should be decreased by 50% and lithium and potassium levels monitored. 

After several months of continuous therapy with lithium, diabetes insipidus and goiter may develop. The kidney tubules then become insensitive to the action of antidiuretic hormone, and its administration is ineffective. Either a dose reduction or discontinuation of the lithium corrects this side effect without leaving any residual pathology. In the... 

A 47-year-old woman, who was taking lithium (serum concentration 0.7 mmol/1) for bipolar I disorder, developed an acute abdominal syndrome (394). She had a recent history of drinking about 4 1 of fluid a day. After surgery, she developed nephrogenic diabetes insipidus, with 19 1/day intake and 15 1/day output. The diuresis fell to 8 1/day over the next 10 days. 

Finch CK, Kelley KW, Williams RB. Treatment of lithium-induced diabetes insipidus with amiloride. Pharmacotherapy 2003 23(4) 546-50. 

Walker RG. Lithium nephrotoxicity. Kidney Int Suppl 1993 42 S93-S98. LamSS, Kjellstrand C. Emergency treatment of lithium-induced diabetes insipidus with nonsteroidal anti-inflammatory drugs. Ren Eail 1997 19 183-188. 

In nephrogenic diabetes insipidus the kidney s ability to respond to AVP is impaired by different causes, such as drugs (e.g. lithium), chronic disorders (e.g. sickle cell disease, kidney failure) or inherited genetic disorders (X-linked or autosomal NDI). This type of diabetes insipidus can not be treated by exogenous administration of AVP or AVP analogues. Instead, diuretics (hydrochlorothiazide combined or not with amiloride) and NSAI (indomethacin) are administrated to ameliorate polyuria. 

The long-term toxic effects of lithium, such as nephrogenic diabetes insipidus, which has been calculated to occur in up to 5% of patients, and the rare possibility of lithium combined with neuroleptics being neurotoxic, has stimulated the research for other drug treatments. However, apart from the neuroleptics, these drugs have not been studied as extensively in the treatment of acute mania, but are worthy of consideration because of their reduced side effects. 

Acquired nephrogenic diabetes insipidus Acquired nephrogenic diabetes insipidus unresponsive to vasopressin has been associated with chronic lithium... 

Both drugs are used in conjunction with other diuretics like thiazide or loop diuretics to augment natriuresis and reduce loss of potassium. Triamterene may be used in the treatment of congestive heart failure, cirrhosis and the edema caused by secondary hyperaldosteronism. Amiloride is also useful in lithium induced diabetes insipidus. 

If serum Na+ is not monitored closely, ADH antagonists can cause severe hypernatremia and nephrogenic diabetes insipidus. If lithium is being used for a psychiatric disorder, nephrogenic diabetes insipidus can be treated with a thiazide diuretic or amiloride. 

When a 45-year-old man with severe lithium-induced diabetes insipidus developed hyperosmolar, nonketotic hyperglycemia, it was suggested that poorly controlled diabetes mellitus may have contributed to the polyuria (684). Prior contact with a female patient who had developed hyperosmolar coma secondary to lithium-induced diabetes insipidus (685) allowed physicians 4 years later to treat her safely after a drug overdose and a surgical procedure, by avoiding intravenous replacement fluids with a high dextrose content (despite stopping lithium several years earlier, the patient continued to put out 10 liters of urine daily) (686). 

Lithium Carbonate Common symptoms of lithium toxicity are nausea, vomiting, and diarrhea followed by tremor, increased muscle tone, and rigidity. Acute kidney problems and nephrogenic diabetes insipidus may be possible hazards. In serious cases, coma and convulsions can be observed along with toxicity. 

Hypernatremia can occur secondary to dehydration in patients taking lithium and is not uncommon in association with lithium poisoning. Lithium-induced diabetes insipidus is often a contributing factor. 

Dehydration, secondary to lithium-induced nephrogenic diabetes insipidus, was thought to be the cause of a superior sagittal sinus thrombosis in a 30-year-old woman who presented with confusion, papilledema, and a left hemiparesis (336). 

Renal size and structure have been evaluated by MRI in 16 patients with renal insufficiency and nephropathy thought to be secondary to lithium (377). There were renal microcysts in all patients. All the patients had nephrogenic diabetes insipidus, in which antidiuretic hormone concentrations are raised, and there is evidence that antidiuretic hormone can stimulate the production of renal cysts, by an action mediated via cyclic AMP (378). 

Nephrogenic diabetes insipidus in a 63-year-old woman was treated successfully with lithium withdrawal and amiloride (395). 

A 76-year-old man developed severe intractable diabetes insipidus which was attributed to lithium (395). He was hospitalized for over 2 weeks and eventually died from intestinal hemorrhage. Vigorous efforts were made to treat his polyuria, electrolyte disturbances, hypernatremia, and dehydration. He had been taking chlorpromazine, lithium, and furosemide, along with other medications, and the diagnosis of lithium-induced nephrogenic diabetes insipidus was considered because of a lack of alternative explanations. 

There have been several case reports of Uthium-related nephrogenic diabetes insipidus, sometimes associated with dehydration and lithium intoxication (216,293-296). 

Nephrogenic diabetes insipidus has been described in patients receiving foscarnet, either alone or associated with a distal renal tubular acidosis [66, 67, 68]. In fact, a recent review cited foscarnet as the second most common reported cause of drug-induced diabetes insipidus, second only to lithium [69]. In experiments using toad urinary bladders [70], serosal application of foscarnet enhanced water flow in the presence of submaximal ADH concentrations, but did not affect water transport in the absence of ADH or when maximal concentrations of ADH were used. Mucosal foscarnet did not affect water transport. Further studies are needed to clarify the mechanisms for altered water handling by the kidneys with foscarnet. 

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